Interaction of silica with human immune cells
Karhinoja, Katri (2018-12-18)
Interaction of silica with human immune cells
(18.12.2018)
Julkaisu on tekijänoikeussäännösten alainen. Teosta voi lukea ja tulostaa henkilökohtaista käyttöä varten. Käyttö kaupallisiin tarkoituksiin on kielletty.
suljettu
Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe201902276502
https://urn.fi/URN:NBN:fi-fe201902276502
Tiivistelmä
Aim of this study was to evaluate silica’s ability to promote inflammation. Amorphous silica could be used in sustained drug delivery systems, but it needs to be proven to be safe.
Neutrophils ability to phagocytose silica microparticles was studied using flow cytometry. Neutrophils were isolated from human blood samples taken from healthy volunteers. Silica’s ability to induce cytokine production was studied by incubating differentiated THP-1 cells with silica microparticles and measuring IL-1β and TNF-α production with enzyme-linked immunosorbent assay (ELISA).
Neutrophils were found to phagocytose silica microparticles in a concentration dependent manner. Particles were phagocytosed most with particle concentration 0.125 mg/ml, but difference between this and higher concentration was not statistically significant.
Silica microparticles did not induce production of TNF-α but might have induced production of IL-1β although positive control for IL-1β was not working properly.
Silica microparticles might promote inflammation but it needs to be further studied with working positive control and with other particles, so silica induced inflammation could be compared.
Neutrophils ability to phagocytose silica microparticles was studied using flow cytometry. Neutrophils were isolated from human blood samples taken from healthy volunteers. Silica’s ability to induce cytokine production was studied by incubating differentiated THP-1 cells with silica microparticles and measuring IL-1β and TNF-α production with enzyme-linked immunosorbent assay (ELISA).
Neutrophils were found to phagocytose silica microparticles in a concentration dependent manner. Particles were phagocytosed most with particle concentration 0.125 mg/ml, but difference between this and higher concentration was not statistically significant.
Silica microparticles did not induce production of TNF-α but might have induced production of IL-1β although positive control for IL-1β was not working properly.
Silica microparticles might promote inflammation but it needs to be further studied with working positive control and with other particles, so silica induced inflammation could be compared.